GHB enhances the cholinergic function by moderating nicotinic ACh receptor and by competitively and reversibly inhibiting AChE. The binding of Galantamine to AChE slows down the catabolism of ACh, resulting in an increase of ACh levels in the synaptic cleft17

eventually leading to increased neural activity. This route enhances the channel activity of the pre-synaptic nicotinic receptors in response to ACh, combined with an enhanced post-synaptic response.18 Galantamine is a reversible and selective AChEI having 50 times more selectivity for human AChE than for human butyrylcholinesterase. Galantamine also acts as a nicotinic receptor agonist in the brain.19 This report further strengthen our observation in the present study where administration of GHB caused elevation in ACh and inhibition AChE levels in mice in the absence of disease. In PCI-32765 chemical structure addition to Galantamine, Rivastigmine has also been observed to improve cognitive function as well as hallucinations in Parkinson’s disease patients.20 Clinically cognitive improvements are seen after 8 weeks of treatment with Galantamine and treatment typically continues for 3–6 months.21 In vivo studies SB203580 ic50 have reported that Galantamine administered for 35 days up regulated the number of nicotine-binding sites in

the brain of rats.22 This enhancement of nicotinic neurotransmission may be clinically relevant because activation of pre-synaptic

nicotinic receptors increases the release of ACh and other neurotransmitters that are deficient in patients with Alzheimer’s disease. Cholinergic systems are critical to the neural mechanisms involved in modulation of various cognitive functions, including arousal, attention, learning and memory. Neuronal nicotinic Ach receptors (nAChRs) are the focus of extensive research due to their involvement in numerous important physiological processes such as cognitive learning and memory, synaptic almost plasticity, and neuroprotection.23 As result, the so-called “cholinergic hypothesis” of AD was proposed. It was based on two central notions: the first was that the forebrain cholinergic system sustains a wide variety of cognitive processes; the second was that a dysfunction of cholinergic neurons in the brain contributes significantly to cognitive decline in AD. AChE inhibition is currently the most established strategy for correcting cholinergic deficits in the hippocampus and cortex24 of Alzheimer’s patients thus improving cognitive symptoms. AChE inhibitors, such as Galantamine, Donepezil, Rivastigmine, Physostigmine and Tacrine, having the property of inducing modest improvement in the cognitive function are commonly used to treat the memory impairments associated with AD,25 specifically against cerebral ischaemia,26 and 27 and also Schizophrenia.